Plus-Hex CLINICAL
Introduction
Gastric dilatation and volvulus( GDV) is a true emergency in practice, for which the veterinary nurse( VN) ought to be prepared. Typically, the patient will present with a history of retching, hypersalivation, a restless demeanour and, most obviously, a distended abdomen. However, GDV patients are not easy to treat and care for, as they are also likely to have a lot of haemodynamic abnormalities that must be addressed.
This article will cover hypovolaemic shock, abnormalities in blood serum lactate and intravenous fluid therapy( IVFT) as relevant to the GDV patient. The aim of this article is to educate VNs on this topic, especially those VNs who do not see this emergency presentation often, to give them confidence in their nursing skills so they can provide the best possible care to the patient.
Learning outcomes
• Understand how the body compensates for fluid loss
• Understand how hypovolaemic shock can cause changes in blood serum lactate
• Know how to select appropriate IVFT and the correct catheter placement for the GDV patient
• Recognise the signs of fluid overload
Hypovolaemic shock
It is important for the VN to understand how the body compensates for fluid loss, because a patient that is admitted with hypovolaemic shock may not initially be hypotensive, due to the body ' s compensatory mechanisms. If the clinical signs of hypovolaemic shock are not addressed as a priority, hypotension will develop once the body ' s compensatory mechanisms become exhausted [ 1 ].
Neural and hormonal mechanisms within the body act to try to achieve an increase in cardiac output and vascular tone to continue supplying the cells with oxygen, to prevent hypoxaemia and hypotension. There are acute, moderate and chronic compensatory mechanisms that function, depending on the patient ' s parameters at the time.
During the acute stage, baroreceptors within the aorta detect a change in the blood pressure, vascular tone and cardiac output. These baroreceptors send a signal to the sympathetic nervous system( SNS), resulting in catecholamines being released within a few minutes. The signals from the SNS will increase and noradrenaline( norepinephrine) is released from the adrenal glands. Noradrenaline binds to α-adrenergic receptors located within the blood vessels, resulting in vasoconstriction.
Noradrenaline also binds to β1-adrenergic receptors located within the myocardium, resulting in increases in the heart rate( HR) and cardiac contractility [ 2 ]. During this stage, the body will also try to compensate for fluid loss through transcapillary shifting of fluid from the interstitial space to the vascular space; this primarily occurs in patients with hypovolaemic shock. A canine patient in the acute stage will have a body temperature of 36.6 – 37.2 ° C, an HR of > 180 bpm and a respiratory rate( RR) of > 50 breaths / min. They will be quiet, alert and responsive, with pale mucous membranes( MMs), a capillary refill time( CRT) of < 1 second and a mean arterial blood pressure( MAP) of 70 – 80 mmHg [ 2, 3 ].
After the acute mechanisms, the body will start to compensate for moderate shock; this usually occurs 10 minutes to 1 hour after entering shock. During this stage, the baroreceptors in the juxtaglomerular apparatus detect a decrease in cardiac output; this leads to a release of renin. Renin is an enzyme produced by the kidneys; it causes angiotensinogen to convert into angiotensin I within the circulation, and angiotensin I is then converted into angiotensin II within the lungs [ 4 ]. Angiotensin II binds to receptors in the blood vessels and causes vasoconstriction; this improves vascular tone, which in turn increases venous return and cardiac output, helping to maintain perfusion to the vital organs [ 2 ]. The posterior pituitary gland located in the brain releases vasopressin in response to the shift of body fluids due to osmosis. Vasopressin is a hormone that acts to increase the reabsorption of water in the collecting ducts of the kidneys and decrease the excretion of water in urine; this will aid the return of blood from the tissues and organs back to the heart and help maintain cardiac output. A dog in this stage will have a temperature in the range of 35.5 – 36.6 ° C, a HR of > 150 bpm and a RR of > 50 breaths / min. It will have obtunded mentation, pale MMs, a CRT < 2 seconds and a MAP of 50 – 60 mmHg [ 2, 3 ].
After the acute and moderate compensatory stages for shock, if the patient has survived, the last stage, chronic compensation, consists of the body trying to replace the lost intravascular volume. This will occur between 1 and 48 hours after the onset of shock. While angiotensin II acts to cause vasoconstriction, it also stimulates the adrenal glands to secrete aldosterone from the adrenal cortex. Aldosterone is important for improving venous return and cardiac output; it achieves this by increasing sodium reabsorption in the distal convoluted tubule in the kidney. Water will follow the movement of sodium by osmosis, and is then reabsorbed into the blood vessels, thus increasing the circulating volume. Another way in which the body improves volaemia is by the release of antidiuretic hormone( ADH); ADH is similar to vasopressin but acts in a different way. ADH binds to the vasopressin 2 receptors located in the collecting ducts of the kidney, which stimulates the placement of aquaporins in the plasma membrane of the epithelial cells in the collecting ducts, thus allowing reabsorption of water. In this stage, a canine patient
Volume 41( 1) • February 2026
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